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Thiamine (vitamin B1), a critical cofactor for carbohydrate metabolism and neurotransmitter synthesis, plays an indispensable role in neuro-ophthalmic health. Deficiency of this crucial nutrient, while traditionally associated with a range of neuro-ophthalmic symptoms, can often lead to clinical presentations that are far from typical. In this case series, we delve into the unique experiences of three young men who developed uncommon neuro-ophthalmic manifestations due to thiamine deficiency following rapid weight loss due to strenuous exercises. Involvement of the optic nerve, presenting as either optic neuritis or papilledema, stands as an unusual revelation of thiamine deficiency; the insidious nature of imaging abnormalities, which require time to manifest, poses an additional diagnostic challenge. It is crucial to recognize that factors such as rapid weight loss and strenuous exercise can precipitate thiamine deficiency, potentially hastening the onset of its neuro-ophthalmic manifestations. Prompt recognition and intervention are essential to mitigate the risk of permanent neurologic deficits, emphasizing the imperative need for awareness and vigilance among healthcare practitioners. Through this series, we aim to augment the understanding of this under-recognized clinical entity.

Peripheral neuropathy is a common manifestation of Eosinophilic Granulomatosis with Polyangiitis (EGPA), a rare autoimmune disorder caused by eosinophilic infiltration of multiple organs including the nervous system. Recent research has shown an association between myelin oligodendrocyte glycoprotein (MOG) antibodies and various neurologic conditions. We present a unique case of EGPA with positive MOG antibodies in the cerebrospinal fluid (CSF) in a patient presenting with peripheral neuropathy. We also highlight a few diagnostic dilemmas with EGPA and the importance of early diagnosis and appropriate treatment. Clinical, laboratory, radiological, and electrophysiologic findings are discussed.

Myelin oligodendrocyte glycoprotein (MOG) antibodies have been identified in central nervous system inflammatory demyelinating disorders (MOG antibody disease), inclusive of optic neuritis, transverse myelitis, or acute disseminated encephalomyelitis. The association of MOG antibodies with combined central and peripheral demyelination (CCPD) is not clear. It has been reported in a few cases where MOG antibodies were detected in the serum of patients with chronic inflammatory demyelinating polyneuropathy. However, multifocal motor neuropathy with MOG antibodies is extremely rare. We present a patient who had clinical, neurophysiological, radiological, and biochemical findings that support the diagnosis of CCPD (multifocal motor neuropathy and cord lesion) with MOG antibodies. The patient was treated with a combination therapy of intravenous immunoglobulins plus high-dose methylprednisolone, which resulted in significant improvement.